Food deprivation alters liver glycogen metabolism and endocrine responses to hemorrhage

Abstract

Liver glycogen content, blood glucose, insulin, glucagon, and epinephrine were determined during 1 h hemorrhagic hypotension at 60 mmHg and 23 h thereafter in fed and two groups of 24-h food-deprived rats receiving either no infusion or 30% glucose intravenously during hemorrhage. Liver glycogen content was reduced by greater than 90% after 24-h food deprivation. Fed and food-deprived rats given glucose developed similar and substantial elevations of blood glucose during hemorrhage, whereas changes in blood glucose were modest in food-deprived rats given no infusion. In fed rats, liver glycogen was reduced by 60% during the 1-h bleed, but within 2 h after hemorrhage repletion of liver glycogen content commenced. By 6 h, approximately 75% of the glycogen lost during hemorrhage had been restored, and 23 h after hemorrhage liver glycogen content was six times greater compared with nonbled controls. Although glycogen levels increased after hemorrhage in food-deprived animals, the increase was negligible compared with that found in fed rats. Infusion of glucose during hemorrhage or adrenergic blockade after hemorrhage did not alter glycogen repletion in food-deprived rats. Posthemorrhage fed animals had high levels of insulin, glucagon, and epinephrine during hemorrhage, whereas insulin levels remained low in food-deprived rats despite exogenously induced hyperglycemia. It is concluded that rapid and substantial glycogen repletion can occur even immediately poststress. The conditions seem to be related to the nutritional state at the time of the insult.

Hemorrhage induces the rapid development of hepatic insulin resistance

“…Although elevation of epinephrine and glucagon can stimulate glycogen breakdown, glycogenolysis is also an unlikely source for the extreme hyperglycemia of the hemorrhaged animals. Previous studies suggest that hepatic glycogen content is reduced over 90% following a 20-to 24-h fast (28). In support of this contention, data from Maitra et al (33) suggest that adrenergic blockers and inhibition of glucagon had no effect on hemorrhage-induced hyperglycemia in rats fasted for 20 h. However, breakdown of liver or muscle glycogen may have contributed to the increase in blood glucose.…”

Physiologic considerations of Enhanced Recovery After Surgery (ERAS) programs: implications of the stress response

“…Data from animals have shown that fasting not only causes a greater endocrine response to hemorrhagic stress but also results in lower survival compared with non-fasted animals. 27,28 The transition to a non-fasted state with a meal or exogenous glucose administration elicits a significant insulin response and also blocks endogenous glucose production. Insulin changes the principal source of metabolism from fat to carbohydrates, thus maintaining protein stores and activating glucose transport into muscle.…”

Perioperative catabolism

“…Under certain conditions, such as a high risk of aspiration or preoperative bowel preparation, fasting periods are long enough to deplete hepatic glycogen stores and, thereby, increase the demand for amino acids for gluconeogenesis rather than tissue repair. [141][142][143][144][145] Animal studies have shown that coping with stress is improved when the animals enter the trauma fed, not fasting. 142 Overnight treatment with glucose prevents postoperative decrease in insulin sensitivity 30,146 and early loss of protein after gastrointestinal surgery [147][148][149] and augments voluntary muscle function.…”